Ontogenetic Development of Neurophysiological Mechanisms Underlying Language Processing

During the last 20 years, new data on the neurophysiological mechanisms underlying different types of cognitive activity, especially speech and its ontogenetic formation, were obtained in the Laboratory of Children’s Neurophysiology headed by Prof. M.N. Tsitseroshin. Using the analysis of the spatial-temporal structure of regional interactions of cortical bioelectric potentials (so-called functional connectivity), we investigated how specific language levels, such as phonology, grammar, and semantics, are represented in the brain. The data obtained in children vs. adults indicate that the speech perception and production require joint and extremely coordinated activities of both hemispheres, along with the obligatory and differentiated involvement of “classic” speech centers in the left hemisphere, especially Wernicke’s area. Another line of our research is to explore the differences, which arise during verbal processing in adults and children with impaired vs. non-impaired speech, particularly with alalia, dysarthria and stuttering, using behavioral and EEG data. Our data obtained in children vs. adults allow assessing the degree of maturity in the organization of the central processes of maintaining the studied types of verbal activity in children of different ages. These data allow expanding modern concepts about the brain mechanisms of verbal activity in children in the norm and pathology

ФАЗОВЫЕ ПРЕВРАЩЕНИЯ ПРИ КРИСТАЛЛИЗАЦИИ Sr2FeMoO6–δ ИЗ ПРОСТЫХ ОКСИДОВ

The sequence of phase transformations during Sr2FeMoO6–δ crystallization by the solid phase method was studied for powders synthesized from the stoichiometric mixture of SrCO3 Fe2O3, MoO3 oxides. It is found that the synthesis of a strontium ferromolybdate solid solution proceeds through a series of parallel chemical reactions. It is revealed that at the beginning stage of interaction, the initially formed Sr2FeMoO6–δ powder is enriched with iron. During the annealing process, the composition of strontium ferromolybdate changes and the molybdenum content increases upon further heating. It is shown that in the process of crystallization of double perovskite in the temperature range T = (300–1420) K, there is the following sequence of phase transformations Fe2O3, MoO3, SrCO3} (300 К) → {SrMoO4, Fe2O3, SrCO3} (770 К) → {SrMoO4, SrFeO3–х (traces), Sr2FeMoO6–δ (traces)} (970 K) → {SrMoO4, Sr2FeMoO6–δ } (1170 К) → { Sr2FeMoO6–δ } (1420 К)..На основании изучения последовательности фазовых превращений при кристаллизации Sr2FeMoO6–δ установлено, что синтез двойного перовскита в смеси простых оксидов протекает через ряд последовательно-параллельных стадий. На начальном этапе взаимодействия образующийся ферромолибдат стронция обогащен железом и его состав в ходе реакции изменяется в сторону увеличения содержания молибдена. Оксид молибдена в тройной смеси состава 2SrCO3+ + MoO3 + 0,5Fe2O3 вступает в реакцию несколько быстрее с карбонатом стронция, чем оксид железа. Показано, что в процессе кристаллизации двойного перовскита ферромолибдата стронция в интервале температур Т = (300–1420)К имеет место следующая последовательность фазовых превращений: {Fe2O3, MoO3, SrCO3} (300 К) → {SrMoO4, Fe2O3, SrCO3} (770 К) → {SrMoO4, SrFeO3–х (следы), Sr2FeMoO6–δ (следы)} (970 К) → {SrMoO4, Sr2FeMoO6–δ } (1170 К) → { Sr2FeMoO6–δ } (1420 К)

Associations between outdoor temperature and markers of inflammation: a cohort study

<p>Abstract</p> <p>Background</p> <p>Associations between ambient temperature and cardiovascular mortality are well established. This study investigated whether inflammation could be part of the mechanism leading to temperature-related cardiovascular deaths.</p> <p>Methods</p> <p>The study population consisted of a cohort of 673 men with mean age of 74.6 years, living in the greater Boston area. They were seen for examination roughly every 4 years, and blood samples for inflammation marker analyses were drawn in 2000-2008 (total of 1254 visits). We used a mixed effects model to estimate the associations between ambient temperature and a variety of inflammation markers (C-reactive protein, white blood cell count, soluble Vascular Cell Adhesion Molecule-1, soluble Intercellular Adhesion Molecule-1, tumor necrosis factor alpha, and interleukins -1β, -6 and -8). Random intercept for each subject and several possible confounders, including combustion-related air pollution and ozone, were used in the models.</p> <p>Results</p> <p>We found a 0 to 1 day lagged and up to 4 weeks cumulative responses in C-reactive protein in association with temperature. We observed a 24.9% increase [95% Confidence interval (CI): 7.36, 45.2] in C-reactive protein for a 5°C decrease in the 4 weeks' moving average of temperature. We observed similar associations also between temperature and soluble Intercellular Adhesion Molecule-1 (4.52%, 95% CI: 1.05, 8.10, over 4 weeks' moving average), and between temperature and soluble Vascular Cell Adhesion Molecule-1 (6.60%, 95% CI: 1.31, 12.2 over 4 weeks' moving average). Penalized spline models showed no deviation from linearity. There were no associations between temperature and other inflammation markers.</p> <p>Conclusions</p> <p>Cumulative exposure to decreased temperature is associated with an increase in inflammation marker levels among elderly men. This suggests that inflammation markers are part of intermediate processes, which may lead to cold-, but not heat-, related cardiovascular deaths.</p

Short-term consumption of a high-fat diet increases host susceptibility to Listeria monocytogenes infection

peer-reviewedBackground A westernized diet comprising a high caloric intake from animal fats is known to influence the development of pathological inflammatory conditions. However, there has been relatively little focus upon the implications of such diets for the progression of infectious disease. Here, we investigated the influence of a high-fat (HF) diet upon parameters that influence Listeria monocytogenes infection in mice. Results We determined that short-term administration of a HF diet increases the number of goblet cells, a known binding site for the pathogen, in the gut and also induces profound changes to the microbiota and promotes a pro-inflammatory gene expression profile in the host. Host physiological changes were concordant with significantly increased susceptibility to oral L. monocytogenes infection in mice fed a HF diet relative to low fat (LF)- or chow-fed animals. Prior to Listeria infection, short-term consumption of HF diet elevated levels of Firmicutes including Coprococcus, Butyricicoccus, Turicibacter and Clostridium XIVa species. During active infection with L. monocytogenes, microbiota changes were further exaggerated but host inflammatory responses were significantly downregulated relative to Listeria-infected LF- or chow-fed groups, suggestive of a profound tempering of the host response influenced by infection in the context of a HF diet. The effects of diet were seen beyond the gut, as a HF diet also increased the sensitivity of mice to systemic infection and altered gene expression profiles in the liver. Conclusions We adopted a systems approach to identify the effects of HF diet upon L. monocytogenes infection through analysis of host responses and microbiota changes (both pre- and post-infection). Overall, the results indicate that short-term consumption of a westernized diet has the capacity to significantly alter host susceptibility to L. monocytogenes infection concomitant with changes to the host physiological landscape. The findings suggest that diet should be a consideration when developing models that reflect human infectious disease.This research was funded by the European Union’s Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie grant agreement No. 641984, through funding of the List_MAPS consortium. We also acknowledge funding and support from Science Foundation Ireland (SFI) in the form of a center grant (APC Microbiome Ireland grant SFI/12/RC/2273)

Fetal and infant origins of asthma

Previous studies have suggested that asthma, like other common diseases, has at least part of its origin early in life. Low birth weight has been shown to be associated with increased risks of asthma, chronic obstructive airway disease, and impaired lung function in adults, and increased risks of respiratory symptoms in early childhood. The developmental plasticity hypothesis suggests that the associations between low birth weight and diseases in later life are explained by adaptation mechanisms in fetal life and infancy in response to various adverse exposures. Various pathways leading from adverse fetal and infant exposures to growth adaptations and respiratory health outcomes have been studied, including fetal and early infant growth patterns, maternal smoking and diet, children’s diet, respiratory tract infections and acetaminophen use, and genetic susceptibility. Still, the specific adverse exposures in fetal and early postnatal life leading to respiratory disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life, and their epigenetic mechanisms may underlie the complex associations of low birth weight with respiratory disease in later life. New well-designed epidemiological studies are needed to identify the specific underlying mechanisms. This review is focused on specific adverse fetal and infant growth patterns and exposures, genetic susceptibility, possible respiratory adaptations and perspectives for new studies

Ambient air pollution and thrombosis

Abstract Air pollution is a growing public health concern of global significance. Acute and chronic exposure is known to impair cardiovascular function, exacerbate disease and increase cardiovascular mortality. Several plausible biological mechanisms have been proposed for these associations, however, at present, the pathways are incomplete. A seminal review by the American Heart Association (2010) concluded that the thrombotic effects of particulate air pollution likely contributed to their effects on cardiovascular mortality and morbidity. The aim of the current review is to appraise the newly accumulated scientific evidence (2009–2016) on contribution of haemostasis and thrombosis towards cardiovascular disease induced by exposure to both particulate and gaseous pollutants. Seventy four publications were reviewed in-depth. The weight of evidence suggests that acute exposure to fine particulate matter (PM2.5) induces a shift in the haemostatic balance towards a pro-thrombotic/pro-coagulative state. Insufficient data was available to ascertain if a similar relationship exists for gaseous pollutants, and very few studies have addressed long-term exposure to ambient air pollution. Platelet activation, oxidative stress, interplay between interleukin-6 and tissue factor, all appear to be potentially important mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes. Overall, the recent literature supports, and arguably strengthens, the contention that air pollution contributes to cardiovascular morbidity by promoting haemostasis. The volume and diversity of the evidence highlights the complexity of the pathophysiologic mechanisms by which air pollution promotes thrombosis; multiple pathways are plausible and it is most likely they act in concert. Future research should address the role gaseous pollutants play in the cardiovascular effects of air pollution mixture and direct comparison of potentially susceptible groups to healthy individuals